EKG and cardiac meds Flashcards by Meghan May

What effect does the PNS have on the heart?

will DECREASE HR when activated via X

no effect on the blood vessels (more SNS activity)

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What is the SNS role in the heart?

from Thoracic and lumbar: key for arteries and veins; causeing vasoconx to increase BP

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What part of the brain plays big role in medulla for autonomic outlfow

NTS for both PNS and SNS

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If you BP rises up really high what baroreceptors are activated? what effect does that have on the heart?

Increased BP will increase firing from baroreceptors–> this results in activating the SNS IHIBITORY pathway to decrease sympathetic ouflow

AND

cause EXCITAITON of PNS to lower HR

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Where is the cell body of the vagus located?

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What can influence CV status?

Inputsthroughcentral pathways can either excite or inhibit medullary CV centers

Emotion, pain, motor activity, etc., can influence cardiovascular status

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What is the key pathophysciology for vasovagal syncope

Prolongued standing–> venous pooling and decreased venous return

Pain/anxiety causing sympathetic surge–> vigous cardiac contraction

Markedely reduced end systolic volume –> vagal reflex!

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What is the vagal reflex

Bradycardia and vasodialtion leading to hypotension and syncope

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What can you do to help person out with Bezold Jarisch reflex

increase fluid status, give Na tablets,

using a beta blocker can trigger event!

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88 yo femaile feels weak and dizzy after passing the fuck out at home

Vent: 43 BPM

PR interval: 32 ms

QRS duration: 146 ms

QT/QTc: 588/497 ms

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whats this shit?

2nd degree type 1

see prolongued PR interval until you eventually drop a beat

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Whats the difference between type 1 and type 2 2nd degree heart block

Both have dropped beats

1: you see prolongued PR till drop a beat
2: you see regularly dropped beats in consistnat ratio

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Whats this

3rd degree block

see inferior STEMI; characteristic tombstone appearance, the P waves beat indof PRS

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83 yo with palpitations after syncopal episode

Vent rate: 300

PR interval: 104

QRS duration: 136ms

Pt/PTc: 132/295

Regular ventricular tachycardia

ventricles because the QRS is wider–> the ventricles are on loop adn beating inde of atria

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44 yo male with hx of pychosis has syncopal episode,now assymptomatic

vent: 73

PR: 208

QRS: 96

QT/QTc: 513/565 ms

Prolongued QT

normal is

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42 yo female, racing heart, syncopal episode, now asymptomatic

Wolf parkinson white

look for delta waves

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What can QT prolongation lead to?

torsades

Overview of EKG and ion channels

Key channels are:

What happens in phase 0 for ventricular myocyte AP

INa with depolarization and fast opening of Na channels as sodium rushes in!

What happens during Phase 1 of ventricle myocyte AP?

(blurp at top of peak)

I_TO transient and d/t K+ channel opening and K+ leaving cell

What happens during Phase 2 (platue phase)

(Platue phase)

I_Ca-L, I_NaCa, I_Kr, I_Ks

key is Na and Ca are both depolarizing and have influx of + charge

this Ca+ flow is causing platue to stay depolarized

What happens during Phase 3 of AP

(Repolarization phase)

I_K channel open, efflux of + charge

What’s going on in Phase 4

(resting phase)

I_k1, I_f

High K and Low Na permeability

If is our funny channel= pacemaker = SA node

What happens if you fuck with the K+ channels?

How does QT prolongation lead to torsades

You end up with increased chance of breaking threshold needed to stimulate beat; Ca++ channel has increased probability of getting reactivated--\> causing action potential

What is the result of a LQT1 or LQT2 from gene deletion

LQT1 (KCNQ1) will decrease Ks LQT2(KCNE1) will decrease Ks these are most prominent; we see smaller K current thus prolongation of QT bc not repolarizing as fast

Dysfnx in LQT3 or LQT8 results in change where?

messes with I_Na (LQT3) I_(Ca) (LQT8) in such a way to INCREASE their influx

What are my Class I Na channel blockers

1A: Quinidine 2A: Lidocaine 3A: fecainide

This drug is an anti-arrythmic works by blocking Na+ channels and K+ channels, thus causes prolongation of QT

Quinidine, Class 1A Na+ blocker

This has a large effect on blocking Na+ thus decresasing depolaization but has no effect on repolarizing current or NO K+ effect

Flecainide

What are the class II antiarrythmics

Beta blockers: propranolol effects diastolic depolarization; most SA and AV nodes with no effect on QT prolongation

What are my class III anti-arrythmics

K+ channel blockers: amiodarone and sotolol amiodarone: can cause QT prolongation adn also inhibits Ca+ and Na+ thus it inhibts the effects QT prolongation would have so won't see Torsades from it Sotolo just affects K channels so do see prolongued QT

What anti-arrythmics are concerning for causing QT pronlongation

Class I: quinidine and procainamide Class 3: sotalol and amiodarone (not as concerning)

What other drugs cause QT prolongation

SSRIs, antipyschotics antibiotics: macrolides, quinolones, fungals like ketoconazole

What ion channel changes cause QT prlongation

Loss of cardiac I_Ks, slowed delayed Loss of function of cardiac I_Kr (rapidly activating delayed rectifyer) Gain of function Cardiac Sodium

Which drugs are okay to use on pt with symptomatic TdP? Lidocaine Fecainide Metoprolol Sotalol

DONT USE SOTALOL

What is the direct effect of vagal nerve stimulation on the CV system

Decreases HR, no effect on force of contraction or LV and no effect on PVR

What methods can we use to dx vasovagal syncope

ECG, Echocardiogrm, tilt-table test holter monitor or implantable loop recorder

Tx options for vasovagal syncope

Non pharm: pt education to avoid triggers, stay hydrated + Na+ Pharm: a1 agonist: midodrine (not great) OR B blockers and fludrocortisone better or pacemaker

most common cause death in young athletes; see syncope in 15-25% pts. See LVH w/out loading and causes outflow obstruction.

Hypertrophic cardiomyopathy

Harsh systolic mumur at apex and lower LSB Increase murmur from squatting to stand Passive leg elevation decreases murmur Echo: see LV wall thick and septal hypertrophy

HCM